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Physiology of the Airways
Published in Anthony J. Hickey, Sandro R.P. da Rocha, Pharmaceutical Inhalation Aerosol Technology, 2019
Anthony J. Hickey, David C. Thompson
Located in the submucosa of cartilage-containing airways and in the lamina propria of the trachea are glands that secrete mucus into the airway lumen (Reid, 1960). Each mucous gland consists of four regions: the ciliated duct, collecting duct, mucous tubules, and secretory tubules (Meyrick et al., 1960). The ciliated duct opens to the lumen of the airways and is lined by ciliated epithelial cells. It merges with the collecting duct, the walls of which comprise columnar cells. Mucous cells line the mucous tubules that lead from the collecting duct. Serous cells (which contribute to the more liquid component of mucus) line the blind-ended serous tubules that are located at the distal ends of the mucous tubules. Several secretory tubules feed into the collecting duct. Mucus is secreted via the collecting and ciliated ducts into the lumen of the airways. Goblet cells, located in the epithelium of the larger central airways, secrete mucus directly into the airway lumen (Rogers, 1994). Mucus hypersecretion results from an increase in the number and/or size of mucous glands and goblet cells in disease states, such as chronic bronchitis (Finkbeiner, 1999; Rogers, 1994).
Air pollution impacts
Published in Abhishek Tiwary, Ian Williams, Air Pollution, 2018
The macrophage then migrates to the terminal bronchiole and is removed from the lung by the mucociliary escalator. All these processes can be overloaded or bypassed under some conditions. The presence of particles stimulates mucus secretion by the goblet cells, although hypersecretion is characteristic of bronchitis. Chronic obstructive pulmonary disease (COPD) and smoking not only lead to hypersecretion of mucus by the goblet cells but also damage the mucociliary escalator. It is currently being suggested that the toxic effects of nanoparticles are a combination of overwhelming the macrophage defences by sheer numbers and the stimulation of oxidant species secretion with their large surface area. Perhaps surprisingly, there is also evidence that inhaled particles can affect organs other than the lungs. For example, there is increased incidence of thrombosis (clots) being formed in either the heart or brain. The mechanism is uncertain, but is believed to involve the production of coagulating chemicals in the blood due to inflammation by particles. Particles may also carry transition metals into the alveolar region, where they catalyse the formation of free radicals and increase oxidative stress.
Responses of humans and other animals
Published in Abhishek Tiwary, Jeremy Colls, Air Pollution, 2017
The macrophage then migrates to the terminal bronchiole and is removed from the lung by the mucociliary escalator. All these processes can be overloaded or bypassed under some conditions. The presence of particles stimulates mucus secretion by the goblet cells, although hypersecretion is characteristic of bronchitis. Chronic obstructive pulmonary disease (COPD) and smoking not only lead to hypersecretion of mucus by the goblet cells but also damage the mucociliary escalator. It is currently being suggested that the toxic effects of nanoparticles are a combination of overwhelming the macrophage defences by sheer numbers and the stimulation of oxidant species secretion with their large surface area. Perhaps surprisingly, there is also evidence that inhaled particles can affect organs other than the lungs. For example, there is increased incidence of thrombosis (clots) being formed in either the heart or brain. The mechanism is uncertain, but is believed to involve the production of coagulating chemicals in the blood due to inflammation by particles. Particles may also carry transition metals into the alveolar region, where they catalyse the formation of free radicals and increase oxidative stress.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
Chronic obstructive pulmonary disease (COPD) patients suffer from chronic airflow obstruction attributed to mucous hypersecretion and persistent inflammation which manifests as chronic bronchitis with or without emphysema (alveolar septal wall destruction). These pathologies lead to wheezing, cough, and dyspnea with acute exacerbations of disease which, if severe, may result in hospitalization and death. COPD also overlaps with asthma in some patients (Postma, Rabe, and Drazen 2015; Zeki et al. 2011), and is associated with pulmonary hypertension and cardiovascular diseases such as systemic hypertension and atherosclerosis (Chaouat, Naeije, and Weitzenblum 2008). Current smokers and those suffering from chronic bronchitis attributed to other environmental exposures exhibit increased mucous (goblet) cell numbers as well as cellular hyperplasia in small and large airways (Mullen et al. 1987; Wright, Ngai, and Churg 1992). In comparison to nonsmokers, smokers display an elevated risk of developing chronic bronchitis and COPD-associated lung ailments, and the extent of symptom exacerbation appears to be associated with host susceptibility (Liu et al. 2010; Raju et al. 2014).
Atmospheric fine particulate matter and epithelial mesenchymal transition in pulmonary cells: state of the art and critical review of the in vitro studies
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Margaux Cochard, Frédéric Ledoux, Yann Landkocz
Asthma is a chronic inflammatory disease characterized by a swelling of pulmonary airways and mucus secretion. This disease affects more than 300 million individuals globally (WHO 2020). Inflammation alone is not sufficient for asthma development. In asthma, an alteration of the airway wall followed by an airway remodeling occurs (Hackett 2012). In asthmatic patients, goblet cells and basal cells distribution increases whereas ciliated cells number fall. Observations such as thickened basal membrane and disruption of adherens and tight junctions were also noted (Gohy et al. 2016). EMT plays a role in the airway remodeling and several markers of EMT were identified in asthmatic epithelium such as ZO-1, E-cadherin and occludin downregulation. Nasal polyps showing a defect of adhesion mechanism were also observed in affected children (Hackett et al. 2009; Nawijn et al. 2011). Type 2 EMT is found in chronic asthma with airway remodeling (Ijaz et al. 2014; Loffredo et al. 2017). It is estimated that 16 million children worldwide are affected by chronic asthma each year attributed to PM2.5 exposure (Anenberg et al. 2018). During PM2.5 pollution peaks, the number of emergency visits increased, especially in asthmatic children (Fan et al. 2016).